“Where the Imaginal Appears Real: A Positron Emission Tomography Study of Auditory Hallucinations.”
Szechtman, Woody, Bowers & Nahmias ; PNAS 1998
The authors on this paper were looking for where in the brain auditory hallucinations are processed to find out why the brain detects them as an external stimulus instead of an internal stimulus. It is a study into how our brains distinguish external auditory input from internal and how this is altered in the hallucination.
Methods
The brain scanner of choice here is the PET scan. Like an fMRI, it measures oxygenated blood in certain areas of the brain as a marker of activity but instead of using the properties of the oxygenated blood itself, it uses radioactive markers in the blood to detect where the oxygenated blood is being directed. The 8 main subjects were all males that were highly hypnotizable and able to have auditory hallucinations while hypnotized. This was all tested for before the experiments. Other subjects they used were those who were hypnotizable but could not have auditory hallucinations. The subjects were monitored under four conditions: thinking of nothing, listening to a tape after being told to listen, imagining they were listening to the tape as vividly possible, and listening to nothing while being told to listen to the tape (the hallucinatory condition). The subjects than rated the clarity of the sounds they hear as well as if they thought it was external or internal.
Results
Figure 1.
Figure 1 a shows the region of the brain activated in the hypnotizable, hallucinating subjects during hearing and hallucinating normalized to the areas activated during imagining and baseline (thinking of nothing). This area is common to both activities and not during imagining or baseline activity. This area of activation is in the ACC. Figure 1b is just a graphical representation to show that baseline and imagining conditions have similar activation while hallucinating and hearing have a similar increase. Figure 1c shows the correlation between activation of the ACC area and the subjects’ responses. The correlation between whether the subject thought the stimulus was external and the activation of the ACC region has a very high correlation coefficient, r= .95, which is a very good correlation. The correlation to clarity and activation is also very linear. This is a pretty good indicator that the increased activity in the ACC is correlated with hallucinations.
The investigators then tested the non-hallucinators and looked at the activation in their brains. Interestingly, they did not have activation in this region which strongly favors the idea that ACC is important for the creation of the hallucination. Instead, the non-hallucinators had activation in the auditory association cortex in both the hearing and the hallucinatory conditions. This is a similar region of activation as in the Hunter paper. They show this region in figure 2.
In Figure 3, they compare hallucinating versus hearing and hallucinating versus baseline for both subject groups. They noticed that not only were the regions activated in the hallucinating group much larger than the non-hallucinators but also that they also had different activation during hearing alone. While both have the auditory cortex activated, the hallucinators have a larger area activated and some of the activation is in the ACC. The authors indicate that this could mean that people who are able to have hallucinations under hypnosis are processing aural information differently than those who do not have these types of hallucinations.
From this data the authors hypothesize that since the ACC is involved with the attention system and since they instruct their subjects to pay attention to an external stimulus (They are told to listen to the tape but then none is played.), that those able to have hallucinations directed the internal event of hearing the tape to an external one. In other words, since they already had their attention directed to an external stimulus, their brains interpreted what they heard as being external.
Both these papers bring strong evidence of how auditory hallucinations are formed. The Szechtman paper shows that subjects that have hallucinations have different activation in their brains than those who do not normally have hallucinations. This activation occurs during hearing and hallucination and includes the ACC. This is important because it provides a link between just activation of the auditory cortex, which also occurs in the non-hallucinating subjects, and the ability to hallucinate. Interestingly, in periods of silence, the Hunter et al show that both the auditory cortex and the ACC can be slightly activated above baseline. The area of activation is actually reduced during hearing compared to silence. From this it seems like there is a regular system in the brain to activate these regions with or without stimulus but it does not lead to hallucinations. External stimulus seems to regulate this activation. But in those susceptible to hallucinations, there is already a baseline difference in hearing external stimulus which increases the activation in the ACC and the auditory cortex. From this, we can speculate that the differences in activation of these regions are leading to hallucinations. I find this particularly interesting because it implies that if one can manipulate these activations (i.e., drugs, stress, hypnosis), anyone could have auditory hallucinations.
